{"title":"Out-of-Hospital Cardiac Arrest in General Population and Sudden Cardiac Death in Athletes","authors":"Bettina Nagy, B. Kiss, Gábor Áron Fülöp, E. Zima","doi":"10.5772/intechopen.101813","DOIUrl":"https://doi.org/10.5772/intechopen.101813","url":null,"abstract":"Sudden cardiac death (SCD) is still one of the leading causes of cardiovascular death in the developed countries. The incidence of out-of-hospital cardiac arrest in Europe varies from 67 to 170 per 100,000 population. The chain of survival will be described in detailed steps. We are going to summarize the treatment options for sudden cardiac arrest from recognition of SCD to resuscitation and post cardiac arrest care. The role of awereness and Automated External Defibrillator and Public Access Defibrillation (AED-PAD) programs will be discussed in brief. SCD is one of the most common causes of death among athletes. Sport can trigger SCD in individuals who already have unknown form of heart disease. Our aim was to detail the underlying causes of SCD in athletes and to identify the possible screening techniques. Existing disease (e.g., myocardial hypertrophy, fibrosis) can be seen as a substrate, and sport as a trigger can cause arrhythmias, increased catecholamine release, acidosis, and dehydration. We will highlight the importance of sports medicine and periodic examination in screening for these conditions. Depending on the etiology, this may include exercise ECG, Holter monitor, CT, MR, echocardiography, and coronagraphy. We are going to conclude the new recommendations for COVID-19 post-infection care for athletes.","PeriodicalId":159289,"journal":{"name":"Cardiac Arrhythmias - Translational Approach from Pathophysiology to Advanced Care [Working Title]","volume":"3 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2022-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"124819445","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Life-Threatening Cardiac Arrhythmias during Anesthesia and Surgery","authors":"Zuraini Md. Noor","doi":"10.5772/intechopen.101371","DOIUrl":"https://doi.org/10.5772/intechopen.101371","url":null,"abstract":"Life-threatening arrhythmias are frequently encountered during anesthesia for cardiac or non-cardiac surgery. They result in a significant cause of morbidity and mortality, particularly in elderly patients. Predisposing factors like electrolytes abnormalities, pre-existing cardiac disease, intubation procedure, anesthetic medications, and various surgical stimulation need to be determined. Early diagnosis and commencement of an appropriate treatment protocol may be lifesaving. Treatment usually involves correction of the underlying causes, cardiac electroversion, and the use of one or more antiarrhythmic agents. Although ventricular tachycardia, ventricular fibrillation, torsade de pointes, and pulseless electrical activity are considered malignant arrhythmias that can lead to cardiac arrest, other types of Brady and tachyarrhythmias are also included in this chapter to enable adopting a more objective approach in the management of arrhythmias intraoperatively, avoiding risks of inappropriate management strategies.","PeriodicalId":159289,"journal":{"name":"Cardiac Arrhythmias - Translational Approach from Pathophysiology to Advanced Care [Working Title]","volume":"1 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2021-11-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"129071245","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"A High Fidelity Transmural Anisotropic Ventricular Tissue Model Function to Investigate the Interaction Mechanisms of Drug: An In-Silico Model for Pharmacotherapy","authors":"Srinivasan Jayaraman, Ponnuraj Kirthi Priya","doi":"10.5772/intechopen.99873","DOIUrl":"https://doi.org/10.5772/intechopen.99873","url":null,"abstract":"A high fidelity transmural anisotropic ventricular tissue model consisting of endocardial, mid myocardial, and epicardial myocytes were configured to investigate drug interaction, such as Hydroxychloroquine (HCQ), under hypoxia conditions without and with pro-arrhythmic comorbidity like hypokalemia in (a) ventricular tissue b) its arrhythmogenesis for different dosages and (b) two different pacing sequences (Normal and tachycardiac). In-silico ventricular modeling indicates HCQ has an insignificant effect on hypoxia with and without comorbidities, except in the combination of mild hypoxia with moderate hypokalemia condition and severe hypoxia with mild hypokalemia where it initiated a re-entrant arrhythmia. Secondly, incorporating drug dosage variations indicates the 10 μM HCQ created PVCs for all settings except in severe hypoxia conditions where re-entrant arrhythmia occurred. In addition to the dosage of HCQ utilized for treatment, the pacing protocol also influences the appearance of re-entrant arrhythmia only for severe hypoxia with 10 μM HCQ dosage alone. For all other conditions, including tachycardiac pacing protocol, no arrhythmia occurred. These findings infer that the arrhythmic fatality rate due to HCQ treatment for hypoxia can be effectively alleviated by subtly altering or personalizing the dosage of HCQ and aid in the treatment of hypoxia-induced symptoms caused by COVID.","PeriodicalId":159289,"journal":{"name":"Cardiac Arrhythmias - Translational Approach from Pathophysiology to Advanced Care [Working Title]","volume":"24 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2021-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"128940149","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The Evolving Concept of Cardiac Conduction System Pacing","authors":"I. Karpenko, Dmytro Skoryi, D. Volkov","doi":"10.5772/intechopen.99987","DOIUrl":"https://doi.org/10.5772/intechopen.99987","url":null,"abstract":"Cardiac pacing is an established treatment option for patients with bradycardia and heart failure. In the recent decade, there is an increasing scientific and clinical interest in the topic of direct His bundle pacing (HBP) and left bundle branch pacing (LBBP) as options for cardiac conduction system pacing (CSP). The concept of CSP started evolving from the late 1970s, passing several historical landmarks. HBP and LBBP used in CSP proved to be successful in small cohorts of patients with various clinical conditions, including binodal disease, atrioventricular blocks, and in patients with bundle branch blocks with indications for cardiac resynchronization therapy. The scope of this chapter is synthesis and analysis of works devoted to this subject, as well as representation of the author’s experience in this topic. The chapter includes historical background, technical, anatomical, and clinical considerations of CSP, covers evidence base, discusses patient outcomes in line with the pros and cons of the abovementioned methods. The separate part describes practical aspects of different pacing modalities, including stages of the operation and pacemaker programming. The textual content of the chapter is accompanied by illustrations, ECGs, and intracardiac electrograms.","PeriodicalId":159289,"journal":{"name":"Cardiac Arrhythmias - Translational Approach from Pathophysiology to Advanced Care [Working Title]","volume":"15 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2021-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"116083859","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Molecular Mechanism and Current Therapies for Catecholaminergic Polymorphic Ventricular Tachycardia","authors":"Bin Liu, Brian D. Tow, Ingrid M Bonilla","doi":"10.5772/INTECHOPEN.98767","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.98767","url":null,"abstract":"The rhythmic contraction of the heart relies on tightly regulated calcium (Ca) release from the sarcoplasmic reticulum (SR) Ca release channel, Ryanodine receptor (RyR2). Genetic mutations in components of the calcium release unit such as RyR2, cardiac calsequestrin and other proteins have been shown to cause a genetic arrhythmic syndrome known as catecholaminergic polymorphic ventricular tachycardia (CPVT). This book chapter will focus on the following: (1) to describing CPVT as a stress-induced cardiac arrhythmia syndrome and its genetic causes. (2) Discussing the regulation of SR Ca release, and how dysregulation of Ca release contributes to arrhythmogenesis. (3) Discussing molecular mechanisms of CPVT with a focus on impaired Ca signaling refractoriness as a unifying mechanism underlying different genetic forms of CPVT. (4) Discussing pharmacological approaches as CPVT treatments as well as other potential future therapies. Since dysregulated SR Ca release has been implicated in multiple cardiac disorders including heart failure and metabolic heart diseases, knowledge obtained from CPVT studies will also shed light on the development of therapeutic approaches for these devastating cardiac dysfunctions as a whole.","PeriodicalId":159289,"journal":{"name":"Cardiac Arrhythmias - Translational Approach from Pathophysiology to Advanced Care [Working Title]","volume":"81 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2021-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"124797341","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}